New research from the Charles Perkins Center of the University of Sydney has discovered a new biological route that could help explain why people with type 2 diabetes are more prone to developing dangerous blood clots, potentially pave the way for future treatments that reduce their cardiovascular risk.
The study, led by the Associate Professor Freda Passam of the Central Clinical School and Associate Professor Mark Larance of the School of Medical Sciences, was published in the Journal of Clinical Investigation. A protein called dry61b has proven to increase considerably in the platelets of people with type 2. Diabetes. The protein seems to disturb the balance of calcium inside the platelets, which makes them more likely to group and form clots.
Above all, researchers have shown that the blocking of dry activity DR61B with an antibiotic – anisomycin – reduces platelets in human samples and animal models.
People living with type 2 diabetes are vulnerable to the increased risk of blood clots. These exciting results identify a whole new way of reducing this risk and helping to prevent potentially deadly complications such as the heart attack and stroke. “”
Associate Professor Freda Passam of the Central Clinical School, University of Sydney
In Australia alone, nearly 1.2 million people lived with type 2 diabetes in 2021. The condition is more widespread in the aboriginal and island peoples of the Torres Strait and in rural and regional communities.
“Cardiovascular disease is a cause of main death in this group, partly due to the increased activity of platelets – the tiny blood cells which help form clots. This sensitivity to increases in coagulation also makes traditional anti-coagulant options less effective in people with type 2 diabetes, limiting options to reduce the risk of cardiovascular disease. »»
The research team used advanced proteomic techniques to study human and mouse pads, discovering that dry61b contributes to calcium leaks from mineral reserves in platelets, which in turn makes the plates more reactive.
While the treatments targeting dry61b are still in the first stages, researchers think that preclinical trials in animals could start in the 1 to 2 years, with potential therapies for patients on the horizon during the next decade.